PM2.5 Induces Angiogenesis Of Bronchial And Lung Tissue In An Allergic Mouse Model

Objective:The overall objective of this study was to evaluate the effect of PM2.5 on angiogenesis of bronchial and lung tissue in an Allergic Mouse Model.Methods:Samples of PM2.5 were collected in Taiyuan, Shanxi Province During 2014.1-2014. 2 and separated into soluble supernatant(Sup) and insoluble precipitate(Pre). Twenty-four male mice were randomly divided into 4 groups: control, asthma, asthma+Sup or asthma+Pre groups(n=6 each). Asthma was induced by intra peritoneal injections of ovalbumin(OVA) and aerosol inhalation of OVA solution. OVA-sensitized mice were exposed via intranasal instilled 25μl of Sup or Pre prior to aerosol inhalation challenge with OVA. Control mice were sensitized and challenged by PBS. After exposure, mice were examined for BALF cell count and IL-1β、IL-5、IL-13、VEGF concentrations. The airway structural and inflammatory changes were assessed by hematoxylin and eosin staining. The protein levels of VEGFR2 in the lung tissues were observed by immunohistochemistry staining.Results:BALF total cell count 、 Lymphocyte and Macrophage cell count, IL-1β、VEGF、IL-5、IL-13 levels, airway wall thickness, angiogenesis, protein expression levels of VEGFR2 were higher in asthma, asthma+Sup or asthma+Pre group compared to control group(P≤0.01). Asthma+Pre group had more Lymphocyte and Macrophage cell count,IL-1β、VEGF levels, airway wall thickness, angiogenesis, protein expression levels of VEGFR2 compared to asthma and asthma+Sup group(P≤0.01). Moreover, asthma+Pre group enhanced expression of VEGFR2 not only in bronchial ciliated epithelium, bronchial smooth muscle layer, and the blood vessel walls, but also the small blood vessels in the lung tissue. However,eosinophil cell count in the asthma and asthma+Sup group were higher than the control and asthma+Pre group(P≤0.01). Conclusions:These findings indicate differential effects of differential PM2.5 fractions in an Allergic Mouse Model.Differences between insoluble particulates and soluble supernatant in inducing airway inflammation, angiogenesis suggest PM2.5 contributes to increased asthma exacerbations by complicated mechanisms.Not only eosinophil but also Th1/Th2 shift are likely involved in this process.